<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.bloodreviews.com/?rss=yes"><title>Blood Reviews</title><description>Blood Reviews RSS feed: Current Issue.    
 
 
 
This respected international journal,  Blood Reviews , is a vital information resource, bringing 
together appraisals of clinical practice, and research from recognized experts. Specially commissioned articles from leading researchers 
and practitioners guarantee truly global coverage of all the sub-specialties of hematology. 
 
 Blood Reviews  publishes review 
articles covering the spectrum of clinical and laboratory haematological practice and research. Although most reviews are invited, the 
editors welcome suggestions from potential authors. They should first write a brief outline of an intended review and send this to Dr 
Trevor Baglin or to Dr Jacob M Rowe. 
   </description><link>http://www.bloodreviews.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2011 Elsevier Ltd. All rights reserved. </dc:rights><prism:publicationName>Blood Reviews</prism:publicationName><prism:issn>0268-960X</prism:issn><prism:volume>26</prism:volume><prism:number>3</prism:number><prism:publicationDate>May 2012</prism:publicationDate><prism:copyright> © 2011 Elsevier Ltd. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.bloodreviews.com/article/PIIS0268960X11000932/abstract?rss=yes"/><rdf:li rdf:resource="http://www.bloodreviews.com/article/PIIS0268960X12000033/abstract?rss=yes"/><rdf:li rdf:resource="http://www.bloodreviews.com/article/PIIS0268960X12000045/abstract?rss=yes"/><rdf:li rdf:resource="http://www.bloodreviews.com/article/PIIS0268960X12000021/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.bloodreviews.com/article/PIIS0268960X11000932/abstract?rss=yes"><title>CNS prophylaxis in diffuse large B-cell lymphoma: If, when, how and for whom?</title><link>http://www.bloodreviews.com/article/PIIS0268960X11000932/abstract?rss=yes</link><description>Abstract: Central nervous system (CNS) relapse is an uncommon devastating complication of diffuse large B-cell lymphoma (DLBCL) that usually occurs within 2years from initial diagnosis. Its pathophysiology is poorly understood and there is no consensus on the definition of high-risk patients for CNS relapse. Consequently, an empirical and highly variable practice of chemoprophylaxis is employed. In this review we critically appraise the available literature in order to address issues related to ineffectiveness of current paradigms of chemoprophylaxis. The commonly used prophylaxis is derived from past experience with childhood acute leukemia where most early CNS relapses are leptomeningeal. In contrast, CNS involvement in DLBCL affects brain parenchyma in almost 60% of cases and thus intrathecal prophylaxis remains ineffective. We propose that CNS relapse in DLBCL is sometimes related to occult malignant cells present in the CNS at diagnosis. In others, CNS relapse is likely due to a later acquisition of CNS-penetrating subtypes of malignant clones. With lack of evidence for occult CNS involvement no strong indication currently exist that any form of chemoprophylaxis is beneficial. Future directions for evaluation and treatment of CNS disease are outlined. This complex and intriguing topic should be ideally investigated by prospective trials.</description><dc:title>CNS prophylaxis in diffuse large B-cell lymphoma: If, when, how and for whom?</dc:title><dc:creator>Tali Siegal, Neta Goldschmidt</dc:creator><dc:identifier>10.1016/j.blre.2011.12.001</dc:identifier><dc:source>Blood Reviews 26, 3 (2012)</dc:source><dc:date>2012-01-16</dc:date><prism:publicationName>Blood Reviews</prism:publicationName><prism:publicationDate>2012-01-16</prism:publicationDate><prism:volume>26</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0268-960X(12)X0003-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>97</prism:startingPage><prism:endingPage>106</prism:endingPage></item><item rdf:about="http://www.bloodreviews.com/article/PIIS0268960X12000033/abstract?rss=yes"><title>Diagnosis and treatment of cold agglutinin mediated autoimmune hemolytic anemia</title><link>http://www.bloodreviews.com/article/PIIS0268960X12000033/abstract?rss=yes</link><description>Abstract: Exact diagnosis of the subtype has essential therapeutic consequences in autoimmune hemolytic anemia. Cold-antibody types include primary chronic cold agglutinin disease (CAD) and rare cases of cold agglutinin syndrome (CAS) secondary to cancer or acute infection. Primary CAD is a clonal lymphoproliferative disorder. Not all patients require pharmacological therapy, but treatment seems indicated more often than previously thought. Corticosteroids should not be used to treat primary CAD. Half of the patients respond to rituximab monotherapy; median response duration is 11months. The most efficient treatment to date is fludarabine and rituximab in combination, resulting in responses in 75%, complete responses in 20% and median response duration of more than 66months. Toxicity may be a concern, and an individualized approach is discussed. Erythrocyte transfusions can be given provided specific precautions are undertaken. No evidence-based therapy exists in secondary CAS, but optimal treatment of the underlying disorder is essential when feasible.</description><dc:title>Diagnosis and treatment of cold agglutinin mediated autoimmune hemolytic anemia</dc:title><dc:creator>Sigbjørn Berentsen, Geir E. Tjønnfjord</dc:creator><dc:identifier>10.1016/j.blre.2012.01.002</dc:identifier><dc:source>Blood Reviews 26, 3 (2012)</dc:source><dc:date>2012-02-13</dc:date><prism:publicationName>Blood Reviews</prism:publicationName><prism:publicationDate>2012-02-13</prism:publicationDate><prism:volume>26</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0268-960X(12)X0003-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>107</prism:startingPage><prism:endingPage>115</prism:endingPage></item><item rdf:about="http://www.bloodreviews.com/article/PIIS0268960X12000045/abstract?rss=yes"><title>Hyperleukocytosis, leukostasis and leukapheresis: Practice management</title><link>http://www.bloodreviews.com/article/PIIS0268960X12000045/abstract?rss=yes</link><description>Abstract: Hyperleukocytosis, arbitrarily defined in acute leukemia as a white blood cell count greater than 100,000/mL, often is associated with increased morbidity and mortality in patients with leukemic processes. It can induce leukostasis, tumor lysis syndrome and disseminated intravascular coagulopathy and has significant prognostic implications with or without one of these clinical complications. The main sites that tend to be injured from the obstructions are the central nerve system and lungs. Despite characteristic clinical presentations, the diagnosis of leukostasis is rarely made with high confidence. The main goal of the management of hyperleukocytosis and/or leukostasis is to reduce the white blood cell count before starting induction chemotherapy. The cytoreduction can be achieved by either leukapheresis and/or hyroxyurea. The technical aspects, complications and efficacy of leukapheresis are discussed in the current article.</description><dc:title>Hyperleukocytosis, leukostasis and leukapheresis: Practice management</dc:title><dc:creator>Chezi Ganzel, Joanne Becker, Paul D. Mintz, Hillard M. Lazarus, Jacob M. Rowe</dc:creator><dc:identifier>10.1016/j.blre.2012.01.003</dc:identifier><dc:source>Blood Reviews 26, 3 (2012)</dc:source><dc:date>2012-02-27</dc:date><prism:publicationName>Blood Reviews</prism:publicationName><prism:publicationDate>2012-02-27</prism:publicationDate><prism:volume>26</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0268-960X(12)X0003-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>117</prism:startingPage><prism:endingPage>122</prism:endingPage></item><item rdf:about="http://www.bloodreviews.com/article/PIIS0268960X12000021/abstract?rss=yes"><title>The clinical relevance of chromosomal and genomic abnormalities in B-cell precursor acute lymphoblastic leukaemia</title><link>http://www.bloodreviews.com/article/PIIS0268960X12000021/abstract?rss=yes</link><description>Abstract: Acute lymphoblastic leukaemia (ALL) occurs at all ages but is the most common cancer of childhood. The current treatment of paediatric ALL is highly successful with up to 90% children being cured. In contrast, survival rates for adult ALL are significantly lower at around 40%. The discovery and characterisation of genetic abnormalities have increased our understanding of the biology of the disease and provided important prognostic and predictive markers which have improved patient outcome. Not only is the spectrum of these aberrations vast but, due to advances in technology, continually expanding. A wide range of chromosomal and genomic abnormalities have been reported as being associated with patient outcome but only a subset are currently used to risk stratify patients. This review highlights the main genetic abnormalities which are used to manage patients with B-cell precursor ALL and discusses the evidence which has been accumulated on several newly described genomic abnormalities.</description><dc:title>The clinical relevance of chromosomal and genomic abnormalities in B-cell precursor acute lymphoblastic leukaemia</dc:title><dc:creator>Anthony V. Moorman</dc:creator><dc:identifier>10.1016/j.blre.2012.01.001</dc:identifier><dc:source>Blood Reviews 26, 3 (2012)</dc:source><dc:date>2012-03-22</dc:date><prism:publicationName>Blood Reviews</prism:publicationName><prism:publicationDate>2012-03-22</prism:publicationDate><prism:volume>26</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0268-960X(12)X0003-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>123</prism:startingPage><prism:endingPage>135</prism:endingPage></item></rdf:RDF>
